The hepatic venous pressure gradient: Anything worth doing should be done right

Abstract

WHVP, wedged hepatic venous pressure; FHVP, free hepatic venous pressure; HVPG, hepatic venous pressure gradient; PVP, portal venous pressure. Over the last two decades, our understanding of the treatment and prognosis of portal hypertension has continued to improve.1, 2 The use of techniques to measure the wedged hepatic venous pressure (WHVP), developed more than 50 years ago, has played a major role in elucidating the pathophysiology of the syndrome3 and, consequently, in developing currently available pharmacologic therapy. Recently, a role for measurements of WHVP has also been proposed in evaluating the progression of chronic liver diseases.4 This measurement has been shown to be the best predictor of the development of complications of portal hypertension in patients with early cirrhosis.5 Investigators in this area of research need not be convinced about the importance of the WHVP technique in advancing our knowledge of portal hypertension from the experimental arena3 to current clinical applications.6-8 However, there is an unanswered question that has lingered with us for more than 20 years: Should measurement of WHVP be incorporated into clinical practice? To begin to answer this question, we must assure ourselves that the technique is executed properly. In a recent study performed to evaluate a new pharmaceutical agent, one of us (R.J.G.) was asked to be a blind reviewer of WHVP tracings performed by centers experienced in the measurement of WHVP. Even though minimal criteria for acceptable measurements have been established (Table 1), approximately 30% of studies% had to be rejected as the tracings obtained were uninterpretable. Our experience is not unique (Jaime Bosch, personal communication). We cannot draw conclusions about the usefulness of this technique in a clinical setting if investigational studies designed to answer the question do not themselves comply with minimal criteria for technical adequacy. To achieve results that are consistent and comparable from center to center, meticulous attention to detail is required (Table 1). 1. Use an appropriate scale. Venous pressures have an upper range of approximately 30–40 mm Hg. Therefore, scales used for arterial pressure measurements are not adequate. To be able to detect small changes, the scale should be set at 1 mm Hg = 1 mm on the scale (or more, e.g., 1 mm Hg = 2.5 mm on the scale; Fig. 2). 5. Check the inflated balloon for total occlusion of the hepatic vein (Fig. 1). If it is not (e.g., venous-to-venous shunts, insufficient inflation of the balloon), the measurements should be repeated either by moving the balloon catheter distal to the venous-to-venous shunts, or, when the drainage is to another hepatic vein, by changing the position of the catheter to another hepatic vein without venous-to-venous shunts. A hepatic vein that drains into another hepatic vein or distal to the balloon occlusion will underestimate the WHVP. In rare cases, the measurement cannot be accomplished. Checking for total occlusion of the balloon (wedged position) should be performed at the end of the measurement by slowly injecting 5 mL of contrast into the hepatic vein while the balloon is inflated. This should show the typical wedged (sinusoidal) pattern and no communication with other hepatic veins. After deflating the balloon the dye should wash out quickly. Do this consistently (i.e., do not check for balloon occlusion before measurements on one procedure and after the measurements in another). Direct measurement of portal venous pressure (PVP) is invasive and inconvenient. In 1951, Myers and Taylor9 first described WHVP, which is the measurement of the sinusoidal pressure, an indirect measurement of PVP. Since then, WHVP has been shown to be very safe and the rate of successful hepatic vein catheterization is greater than 95%. By threading a small catheter into a hepatic vein until it cannot be advanced further, a "wedged" hepatic venous pressure is obtained. As the hepatic vein is occluded, a continuous column of fluid between the catheter and the sinusoid is formed, resulting in a pressure reading that is equal to the sinusoidal pressure (Fig. 1). In normal livers, the low-resistant sinusoidal network dissipates most of the pressure back up from the wedged catheter. As there is no direct connection, via a static column of fluid, between the catheter and the portal tributaries, the pressure reading of the transducer reflects sinusoidal pressure (in normal livers is slightly lower than portal pressure). This is also observed in presinusoidal causes of portal hypertension such as schistosomiasis or early primary biliary cirrhosis. Because the catheter in these cases is not in continuity with the area of increased resistance, the recorded pressure will be that of the normal sinusoids and not of the increased pressure in the portal vein. In these cases, WHVP will be an underestimation of the PVP.11, 12 Conversely, in alcoholic cirrhosis and in most cases of